Literature DB >> 6787554

Liver glycogenosis caused by a defective phosphorylase system: hemolysate analysis.

C Baussan, N Moatti, M Odievre, A Lemonnier.   

Abstract

Investigated were 24 cases of glycogenosis caused by a reduction in liver phosphorylase activity. The intravenous glucagon tolerance test could not discriminate between phosphorylase kinase deficiency [glycogen storage disease (GSD) IX] and phosphorylase deficiency (GSD VI). These two subgroups were distinguished by hemolysate enzyme assays: (1) GSD IX was characterized by a residual phosphorylase kinase activity, a low activation curve for endogenous phosphorylase b and increased amylo-1,6-glucosidase activity. (2) GSD VI was characterized by a normal or increased phosphorylase kinase activity, a slight activation of endogenous phosphorylase b and a normal amylo-1,6-glucosidase activity.

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Year:  1981        PMID: 6787554

Source DB:  PubMed          Journal:  Pediatrics        ISSN: 0031-4005            Impact factor:   7.124


  4 in total

Review 1.  Phosphorylase b kinase deficiency in man: a review.

Authors:  I E Van den Berg; R Berger
Journal:  J Inherit Metab Dis       Date:  1990       Impact factor: 4.982

2.  The natural history of liver glycogenosis due to phosphorylase kinase deficiency: a longitudinal study of 41 patients.

Authors:  P J Willems; W J Gerver; R Berger; J Fernandes
Journal:  Eur J Pediatr       Date:  1990-01       Impact factor: 3.183

3.  Phosphorylase kinase in leukocytes and erythrocytes of a patient with glycogen storage disease type IX.

Authors:  N Bashan; R Potashnik; T Ehrlich; S W Moses
Journal:  J Inherit Metab Dis       Date:  1987       Impact factor: 4.982

4.  Use of platelets, mononuclear and polymorphonuclear cells in the diagnosis of glycogen storage disease type VI.

Authors:  N Dahan; C Baussan; N Moatti; A Lemonnier
Journal:  J Inherit Metab Dis       Date:  1988       Impact factor: 4.982

  4 in total

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